Saturday 30 October 2010

MRCP revision battle 37.1: TB

Today has a respiratory feel....

MRCP revision battle 37.1: TB
MRCP revision battle 37.2: DVT/PE in pregnancy
MRCP revision battle 37.3: Asthma
MRCP revision battle 37.4: Cor pulmonale
MRCP revision battle 37.5: alpha-1 antitrypsin deficiency
MRCP revision battle 37.6: Cystic fibrosis
MRCP revision battle 37.7: HPOA

MRCP revision battle 37.1: TB

TB is an infection caused by mycobacterium tuberculosis.  Primary infection is usually in the lungs (ghon focus, usually in the mid or lower zones).  Second favourite site for primary infection = GI, ileocaecal area.

Incidence =7000/yr in UK

Spread is by droplet infection. Household contacts have 1 in 4 chance of infection therefore contact tracing is very important and TB is a notifiable disease.

Primary TB is often symptomless. Although it may cause fever, sweats, anorexia, cough or erthyema nodosum.  If the immune system ‘wins’, the TB is walled off by calcification; however, the TB remains active in ~ 20% calcified areas and may be reactivated when immune system is weakened, eg steroids, diabetes, HIV.

Post-primary TB makes you ill – fever, malaise, weight loss, anorexia, tiredness, cough, haemoptysis, rarely night sweats.

 It can spread to:
  • brain = meningeal TB
  • spine = Potts fracture
  • blood = miliary
  • skin = lupus vulgaris

•    CXR
•    Sputum cultured/stained with Zielh-Nielsen – looking for acid-fast bacilli
•    Mantoux test of little help in the UK due to BCG

BCG = bacilli calmette-guerin – decreases risk of TB by 50%

Treatment: DOTS
•    2 months rifampicin, isoniazid, pyrazinamide and ethambutol (=RIPE)
•    then 4 months rifamicin and isoniazid
•    Pyridoxine throughout to protect against neuropathic effects of isoniazid

MRCP (and real life) side effects of TB meds to be aware of:

Rifampicin turns bodily excreations orange
Isoniazid and rifampicin cause cirrhosis – check LFTs
Pyrazinamide decreases urea excreation = risk of gout and CI in gout sufferers
Ethambutol can affect the optic nerve - check colour vision

On to DVT and PE in pregnancy...

MRCP revision battle 37.2: DVT/PE in pregnancy

It is one of those unfortunate situations: pregnancy makes DVT/PE more likely (increases risk around 6x), but the presence of a fetus also makes your preferred investigative tests more risky.

Risk is more increased if:
  • >35 yrs
  • higher parity
  • raised BMI
  • smoker
  • sickle cell
  • anaemic
  • dehydration
  • not blood group O

The consensus on management of ?PE in pregnancy seems to be:
  • CXR in all cases
  • compression doppler in all cases - if this shows DVT you can just treat without needing to investigate further

In terms of the next investigation if you clinically suspect PE but the doppler is normal there is a lack of consensus:
  • CTPA delivers 10-30% less radiation to the fetus but
  • V/Q scan causes less radiation to the maternal breast tissue

In general CTPA seems to 'win'

Note that d-dimer is usually 'normal' in the first trimester of pregnancy, rises in the second to third and then returns to baseline at 4-6 weeks post-partum.  However, it is generally not recommended as an investigation in pregnant women.

Treatment for DVT/PE in pregnancy is LMWH, continued for 6 months (with at least 6 weeks of anticoagulation post-partum)

For the really keen:

Next... MRCP revision battle 37.3...

MRCP revision battle 37.3: Asthma

Asthma is a condition characterised by periods of dyspnoea, cough and wheeze caused by reversible airways obstruction.

Asthma diagnosis

The table below (from the 2009 BTS/SIGN guidelines) lists the factors that increase or decrease the probability of the presentation being asthma:

If from history/examination you believe there is a:
  • high probability the patient has asthma --> being a trial of treatment
  • intermediate probability of asthma --> perform spirometry:
    • FEV1/FVC <0.7 - trial asthma treatment
    • FEV1/FVC >0.7 - refer to specialist

After a trial of treatment >400mls improvement in FEV1 or PEFR >15% is significant

In a peakflow diary, look for diurnal variation >25%

Treatment of asthma

Treatment of asthma follows a stepwise approach (BTS/SIGN guidelines):

  1. Mild intermittent asthma
    •  SABA (short-acting inhaled beta 2 agonist) PRN 
    • salamol, salbutamol
  2. Regular preventor therapy
    • corticosteroid 200-800mcg per day
    • beclometasone, fluticasone, budesonide
  3. Initial add-on therapy
    • LABA (long-acting inhaled beta 2 agonist (eg salmeterol))
    • if this doesn't work, stop and trial an oral therapy such as leukotriene receptor antagonist or theophylline
  4. Persistant poor control
    • increase steroid inhaler up to 2000mcg per day
    • add leukotriene receptor antagonist or theophylline
  5. Continuous or frequent oral steroids

If stable for 3 months, consider stepping down a step.

Severity of asthma

In acute asthma attacks, severity may be graded as follows:

  • unable to complete sentences
  • RR>25
  • PEFR<50% predicted or best
  • pulse >110

  • silent chest
  • PEFR <33% predicted or best
  • bradycardia
  • hypotension
  • normal or raised CO2
  • exhaustion

Management of acute severe asthma

Think 'O! sip Ma':
  • high flow oxygen
  • 5mg salbutamol neb
  • 500mcg ipratropium neb
  • 30mg prednisolone (or 100mg hydrocortisone IV)
  • magnesium 1.2g and aminophylline if still not improving
And make sure ITU know if things aren't going well....

Now for a battle with cor pulmonale...

MRCP revision battle 37.4: Cor pulmonale

Cor pulmonale is right heart failure caused by chronic pulmonary hypertension

Normal pulmonary artery pressure = 15mmHg.
Pulmonary hypertension = pulmonary artery pressure >25mmHg at rest or >30mmHg on exercise

Causes of cor pulmonale include:

  • lung disease - of which COPD is by far the commonest
  • pulmonary vascular disease - PE
  •  rib cage deformity

Presentation is:
  • dyspnoea
  • fatigue
  • syncope

  • raised JVP, a and v waves
  • RV heave
  • loud P2
  • pansystolic murmur - tricuspid regurgitation
  • peripheral oedema
  • hepatomegaly
  • Graham Steell murmur = high-pitched early diastolic murmur, best heard 2nd left intercostal space with pt in full inspiration = pulmonary regurgitation

  • CXR
  • FBC - look for secondary polycythaemia
  • ECG - R axis deviation, right ventricular hypertrophy

  • treat cause
  • treat symptoms
  • ?heart-lung transplant

Next up: alpha-1 antitrypsin deficiency

MRCP revision battle 37.5: alpha-1 antitrypsin deficiency

alpha-1 antitrypsin is a serine protease inhibitor produced in the liver.

In the lung it prevents neutrophil elastase from breaking down the alveolar wall.
It is inactivated by cigarette smoke.

Genetic varients of alpha-1 antitrypsin exist and are labelled based on their electrophoresis mobility, with M (medium), S (slow) and Z (very slow).  MM is 'normal' while 'ZZ' has the worst prognosis with panlobular emphysema.

Patients with an alpha-1 antitrypsin defiency are likely to develop COPD early (even without smoking) and liver cirrhosis is common.

Now for a very straightforward battle - cystic fibrosis

MRCP revision battle 37.6: Cystic fibrosis

CF is an autosomal recessive genetic disorder which results in a mutation of CFTR, leading to Cl not leaving cells and so more Na and water entering, resulting in thick, sticky secreations.

The mutation is on chromosome 7.  70% are ΔF5O8

Incidence = 1/2000.  Carriers = 1/25

Presentation in neonates is failure to thrive, meconim ileus or rectal prolapse.
Later presentation tends to be recurrent respiratory infections, cough, wheeze, bronchiectasis.  85% have steatorrhoea.

Signs include:
-    cyanosis
-    clubbing
-    bilateral course crackles

Diagnosis is by pilocarpine sweat test.  Na/Cl>60mmol/l, usually Cl>Na.  CXR may show bronchietasis.  PCR can pick up 90% of mutations.  Faecal elastase is a good screening tool for exocrine pancreatic dysfunction.  Spirometry shows obstruction.

Treatment is MDT, physio, enzyme replacement, heart/lung transplant.

Complications include  
  • diabetes (1/3) 
  • gallstones
  • cirrhosis
  • OP
  • male infertility (no vas deferens or epididimus)
  • vasculitis
  • nasal polyps (1/3) 
  • HPOA (if you don't know what this is you will by the end of the next battle)
  • infections
    • s.aureus
    • h.influenzae
    • pseudomonas
    • s.pneumoniae
    • burkholderia cepacia (gram negative)
    • aspergillos

It tends to be the upper lobes of the lungs that are damaged.

Mean age of death ~30.

So to the final battle of the day, HPOA...

MRCP revision battle 37.7: HPOA

HPOA = hypertrophic pulmonary osteoarthropathy is a paraneoplastic syndrome consisting of periostitis, arthritis and clubbing.

It is seen in around 50% of patients with mesothelioma.

Of the 'usual' lung cancers it is most commonly associated with adenocarcinomas and least commonly associated with small cell lung cancer.

Thats it for today